TESTING THE VALIDITY OF ADULT ATTENTION DEFICIT DISORDER

描述(改编自申请人的摘要)： 尽管媒体的关注度越来越高，成年人的注意力缺陷多动症 无序(ADHD)尚未在大样本中得到系统研究。AS 因此，该领域一直存在关于ADHD有效性的争论 在心理健康诊所就诊的成年人中。来阐明这一点 辩论，我们建议在成人ADHD的一个领域检验假设 很少受到关注：它的遗传流行病学。正如我们在 背景部分，只有两个小规模的试点研究 注意缺陷多动障碍的遗传流行病学。这些数据对于验证 综合症，创建适合发育的诊断算法和 为遗传连锁研究奠定了临床基础。为了填满这个 在研究文献中的差距，我们将解决成人ADHD的有效性 从遗传流行病学的角度来看，通过测试以下几项 我们建议的五个主要目标的假设：1)评估 成人多动症的家族性传播；2)成人多动症的验证 分子遗传学资料；3)成人ADHD的发散效度评估； 4)利用家庭研究数据验证成人ADHD诊断模型； 5)为未来的随访和分子遗传学创造资源 成人多动症的研究。为了实现这些目标，我们将完成两项- 140个ADHD家系和120个对照家系的盲家系研究 我们认为我们的家庭学习战略是一项有价值的投资 有几个原因。一项关于成人多动症的大型双盲研究从来没有 以前就做过了。此外，由于一贯的积极关联一直是 儿童多动症与两个多巴胺相关基因之间的研究报告 收集分子遗传数据将使我们能够确认成人ADHD 在分子水平上。因为我们正在收集有关生命周期的数据 精神病学诊断，我们将能够确定其他障碍是否可以 ADHD的家族性传播或其分子遗传学 联想。我们还将能够评估发病年龄标准。 应该使用什么症状阈值来诊断 成人ADHD，将能够定义表型和样本选择 将最大限度地提高未来连锁研究的收益的规则。要最大化地 这项提议的科学成果，我们将为 成人ADHD的未来分子遗传学和随访研究。我们会设置 这些研究的阶段通过1)提供全面的基线 对后续研究的评估和2)澄清 分子遗传学所需的表型和样本量 学习。因此，如果成立，我们预计拟议的工作将导致 一个既能澄清病因学复杂性的研究计划 并阐明作为成人ADHD危险因素的基因的性质 这是一种混乱。

DESCRIPTION (Adapted from applicant's abstract): Despite increasing media attention, adult Attention-deficit-hyperactivity disorder (ADHD) has not been systematically studied in large samples. As a result, there has been a debate in the field about the validity of ADHD in adults presenting at mental health clinics. To shed light on this debate, we propose to test hypothesis in one domain of adult ADHD that has received scant attention: its genetic epidemiology. As we review in the background section, there have been only two small pilot studies of the genetic epidemiology of ADHD. Such data are essential to validating the syndrome, creating developmentally appropriate diagnostic algorithms and laying the clinical foundation for genetic linkage studies. To fill this gap in the research literature, we will address the validity of adult ADHD from the genetic epidemiological perspective by testing the following hypothesis for the five main aims of our proposal: 1) Assessing the Familial Transmission of Adult ADHD; 2) Validating Adult ADHD with Molecular Genetic Data; 3) Assessing the Divergent Validity of Adult ADHD; 4) Using Family Study Data to Validate Diagnostic Models of Adult ADHD; AND 5) Creating a Resource for Future Follow-up and Molecular Genetic Studies of Adult ADHD. To acheive these aims, we will complete a double- blind family study of 140 ADHD families and 120 control families. We view our family study strategy as being a valuable investment for several reasons. A large double-blind study of adult ADHD has never been done before. Moreover, because consistent positive associations have been reported between childhood ADHD and two dopamine related genes, the collection of molecular genetic data will allow us to validate adult ADHD at the molecular level. Because we are collecting data about lifetime psychiatric diagnoses, we will be able to determine if other disorders can account for the familial transmission of ADHD or its molecular genetic associations. We will also be able to assess what age at onset criterion and what set of symptom thresholds should be used for the diagnosis of adult ADHD and will be able to define phenotypes and sample selection rules that will maximize the yield of future linkage studies. To maximize the scientific yield of this proposal, we will create a resource for future molecular genetic and follow-up studies of adult ADHD. We will set the stage for these studies by 1) providing a comprehensive baseline assessment for a follow-up study and 2) clarifying the nature of phenotypes and the sample sizes that will be needed for molecular genetic studies. Thus, if founded, we expect that the proposed work will lead to a program of research that can both clarify the nosological complexities of adult ADHD and clarify the nature of genes that are risk factors for the disorder.